Ultraviolet radiation (UV) has been established to cause a modification in murine immune responsiveness to certain types of syngeneic tumor transplants. The majority of tumors induced by chronic (UV) exposure are immunologically rejected by normal syngeneic recipients. Subcarcinogenic exposure of prospective tumor recipients to UV prior to transplant, however, renders them susceptible to progressive tumor growth. This alteration in immune function is not due to a panimmunosuppression as evidenced by normal immunologic potential of UV irradiated animals. One mechanism which appears to be operative in this system is the ability of UV to induce the generation of a population of suppressor lymphocytes having the ability to interfere with normal antitumor immunity. The cell type responsible for this effect has been established to be a nylon-wool nonadherent, short-lived, extremely radio-sensitive T-lymphocyte with an apparent specificity for a group of antigens present on all UV-induced tumors tested to date. We are currently investigating the cell type responsible for the inhibition of antitumor responses. Studies are underway to establish the Ly phenotype and presence of Ia (I-J) antigenic markers on the responsible cell type. Using in vitro methodology we are also investigating the cellular requirements and interactions necessary for cytotoxic lymphocyte development with hopes of better understanding the relationship between effector cell, helper T cell, and suppressor T-cell interactions in this interesting tumor-host relationship.